Overview
Definition:
Hypertensive crisis (HTN-C) in children refers to a sustained and severe elevation in blood pressure (BP) that poses an immediate risk of target organ damage
When secondary to underlying renal disease, it implies a direct link between kidney pathology and the acute rise in BP, often due to volume overload, activation of the renin-angiotensin-aldosterone system (RAAS), or impaired nitric oxide production.
Epidemiology:
HTN-C in pediatrics is less common than in adults, with incidence varying based on the underlying cause
Renal disease is a leading cause of secondary hypertension in children, contributing significantly to HTN-C presentations in EDs
Conditions like acute glomerulonephritis, chronic kidney disease (CKD), and renovascular disease are prominent etiologies.
Clinical Significance:
Prompt recognition and management of HTN-C secondary to renal disease are crucial to prevent irreversible end-organ damage, including encephalopathy, retinopathy, cardiac failure, and acute kidney injury progression
This condition is a high-yield topic for DNB and NEET SS examinations due to its critical nature and complexity.
Clinical Presentation
Symptoms:
Headache, often severe and throbbing
Visual disturbances such as blurred vision or transient blindness
Neurological symptoms including lethargy, confusion, seizures, or focal deficits
Chest pain or shortness of breath suggestive of myocardial ischemia or pulmonary edema
Nausea and vomiting
Epistaxis or hematuria may be present if related to underlying renal pathology.
Signs:
Markedly elevated systolic and diastolic blood pressure readings, often >95th percentile for age and height, or >120/80 mmHg in neonates
Fundoscopic examination may reveal papilledema, hemorrhages, or exudates
Cardiovascular findings can include a loud S2, gallop rhythm, or signs of heart failure
Neurological signs may range from altered mental status to focal neurological deficits
Peripheral edema may be present.
Diagnostic Criteria:
A sustained BP reading of >95th percentile for age, sex, and height on at least two occasions
Alternatively, a systolic BP >180 mmHg or diastolic BP >120 mmHg in infants and children, or >140/90 mmHg in neonates, particularly when associated with signs or symptoms of target organ dysfunction, constitutes a hypertensive urgency or emergency.
Diagnostic Approach
History Taking:
Detailed history of previous BP readings, duration of hypertension, and associated symptoms
Inquire about a history of renal disease, urinary tract infections, congenital anomalies, or family history of hypertension or renal disease
Medication history, including use of nephrotoxic agents
Recent onset of swelling, decreased urine output, or hematuria
Presence of neurological, visual, or cardiac symptoms.
Physical Examination:
Accurate serial BP measurements in both upper and lower extremities using appropriately sized cuffs
Comprehensive neurological examination, including assessment of mental status, cranial nerves, and motor/sensory function
Ophthalmoscopic examination for hypertensive retinopathy
Cardiovascular assessment for murmurs, gallops, and signs of fluid overload
Palpation for abdominal masses (e.g., Wilms tumor) or bruits suggestive of renovascular disease
Examination for peripheral edema.
Investigations:
Urinalysis: Proteinuria, hematuria, casts (e.g., red blood cell casts in glomerulonephritis)
Serum creatinine and BUN: To assess renal function and detect AKI or CKD
Electrolytes: Including sodium, potassium, and bicarbonate
Complete blood count (CBC): To detect anemia or signs of infection
Echocardiogram: To assess for left ventricular hypertrophy, diastolic dysfunction, or other cardiac sequelae
Renal ultrasound: To evaluate kidney size, morphology, detect masses, or hydronephrosis
Doppler ultrasound of renal arteries: To assess for renovascular stenosis
ECG: To detect signs of acute ischemia or LVH
Toxicology screen if drug-induced hypertension is suspected
Plasma renin activity and aldosterone levels if primary hyperaldosteronism is considered.
Differential Diagnosis:
Other causes of pediatric hypertension including essential hypertension, coarctation of the aorta, endocrine causes (pheochromocytoma, Cushing's syndrome), and iatrogenic causes (medications)
Distinguishing between hypertensive urgency (severely elevated BP without target organ damage) and hypertensive emergency (severely elevated BP with acute target organ damage) is critical.
Management
Initial Management:
Immediate BP reduction is the priority in hypertensive emergencies
Gradual reduction is preferred to avoid hypotension and hypoperfusion, typically aiming for a 25% reduction in MAP within the first hour, followed by slower reduction over 2-24 hours
Continuous BP monitoring via arterial line is ideal.
Medical Management:
Intravenous (IV) antihypertensive agents are used
For renal disease-related HTN-C, agents that do not significantly impair renal perfusion are preferred
Common choices include: Labetalol (IV infusion or bolus), Nicardipine (IV infusion), or Fenoldopam (IV infusion, a dopamine-1 agonist with renal vasodilator effects)
Hydralazine may be used cautiously but can cause reflex tachycardia and has variable bioavailability
Sodium nitroprusside can be used for severe emergencies but requires careful monitoring due to cyanide toxicity risk
Oral agents like nifedipine (short-acting) are generally avoided due to risk of precipitous BP drops.
Surgical Management:
Surgical intervention is typically reserved for specific underlying renal pathologies causing hypertension, such as: surgical correction of renal artery stenosis (e.g., angioplasty with stenting or bypass), nephrectomy for unilateral renal lesions causing significant hypertension, or tumor resection (e.g., Wilms tumor, pheochromocytoma)
These are usually not emergent procedures unless the HTN-C is directly attributable to an acute surgical complication.
Supportive Care:
Fluid management is critical
avoid fluid overload in patients with compromised renal function
Strict fluid balance monitoring
Continuous cardiac and neurological monitoring
Management of associated complications like seizures with benzodiazepines
Nutritional support, especially if oral intake is compromised.
Complications
Early Complications:
Hypertensive encephalopathy leading to seizures, stroke, or coma
Acute myocardial infarction or heart failure
Aortic dissection
Retinopathy with vision loss
Acute kidney injury progression or irreversible renal damage
Posterior reversible encephalopathy syndrome (PRES).
Late Complications:
Chronic kidney disease progression
End-stage renal disease requiring dialysis or transplantation
Long-term cardiovascular sequelae including LVH and diastolic dysfunction
Persistent visual impairment
Cognitive deficits.
Prevention Strategies:
Aggressive management of underlying renal disease
Regular BP monitoring in children with known renal conditions
Strict adherence to prescribed antihypertensive medications
Education of caregivers on medication compliance and recognition of HTN-C symptoms
Avoidance of nephrotoxic agents
Prompt diagnosis and treatment of urinary tract infections and other causes of acute kidney injury.
Prognosis
Factors Affecting Prognosis:
The severity and duration of the hypertensive crisis
The extent of target organ damage at presentation
The underlying cause of renal disease
The promptness and efficacy of treatment
The presence of comorbidities.
Outcomes:
With prompt and appropriate management, HTN-C can be stabilized, preventing immediate life-threatening complications
However, long-term prognosis is often dictated by the underlying renal disease, with many children requiring ongoing antihypertensive therapy and renal support
Early intervention significantly improves outcomes and reduces the risk of long-term sequelae.
Follow Up:
Close follow-up with pediatric nephrology is essential
Regular BP monitoring, assessment of renal function (serum creatinine, BUN, urinalysis), and cardiac evaluation
Management may require titrating antihypertensive medications, dietary modifications (low sodium), and consideration of renal replacement therapy if indicated
Long-term surveillance for cardiovascular and renal complications is vital.
Key Points
Exam Focus:
Remember the BP thresholds for hypertensive crisis in different pediatric age groups
Prioritize rapid but controlled BP reduction in hypertensive emergencies
Labetalol and nicardipine are first-line IV agents
Fenoldopam offers renal benefits
Suspect renal causes in children presenting with HTN-C, especially if accompanied by hematuria, proteinuria, or edema
The management goal is not normalization, but controlled reduction to prevent end-organ damage.
Clinical Pearls:
Always measure BP in both arms and legs in children with suspected HTN-C
Consider a continuous infusion for titratable BP control over intermittent boluses
Monitor for signs of hypoperfusion after BP lowering
Involve pediatric nephrology early in management
Treat the underlying cause of renal dysfunction vigorously alongside BP control.
Common Mistakes:
Over-lowering BP too rapidly, leading to hypoperfusion and potential organ ischemia
Underestimating the severity of hypertension or failing to recognize signs of end-organ damage
Inadequate fluid management, especially in the presence of renal impairment
Relying solely on oral medications in a hypertensive emergency
Failing to investigate thoroughly for the underlying cause of renal disease.